The clarification and control of the mechanism. concerning metastasis and invasion in colorectal cancer.

在这项研究中，我们研究了c- kit受体（kit）信号转导在结直肠癌细胞增殖和侵袭中的作用。通过RT-PCR、Western blot和流式细胞术检测，我们发现c- kit在两种结直肠癌细胞系中均有表达。在KIT阳性细胞系中，KIT被干细胞因子（stem cell factor， SCF）激活。WST-1增殖试验表明，SCF增强了阳性细胞系的细胞增殖。此外，SCF增强了kit阳性细胞系的侵袭能力。Western blot结果显示，SCF刺激上调p44/42丝裂原活化蛋白激酶（MAPK）和Akt。我们研究了p44/42 MAPK和磷脂酰肌醇3-激酶(PI3K)/Akt通路在细胞增殖和侵袭中的作用。PI3K/Akt活性与细胞增殖和侵袭密切相关，而p44/42 MAPK仅与侵袭相关。综上所述，scf增强kit阳性结直肠癌细胞的增殖和侵袭主要通过PI3K/Akt通路实现。

In this study, we examined the role of c- kit receptor (KIT) signal transduction on the proliferation and invasion of colorectal cancer cells. We found that c- kit was expressed in two colorectal cancer cell lines as determined by RT-PCR, Western blot and flow cytometry. In KIT-positive lines, KIT was activated by stem cell factor (SCF). SCF enhanced cellular proliferation of positive lines as demonstrated by the WST-1 proliferation assay. Furthermore, SCF enhanced the invasive ability of KIT-positive cell lines. SCF stimulation upregulated p44/42 mitogen-activated protein kinase (MAPK) and Akt as shown by Western blot. We examined the roles played by p44/42 MAPK and phosphatidylinositol 3-kinase (PI3K)/Akt pathways in proliferation and invasion. PI3K/Akt activity strongly correlated with proliferation and invasion while p44/42 MAPK was correlated with only invasion. In conclusion, the SCF-enhanced proliferation and invasion of KIT-positive colorectal cancer cells is achieved mainly through the PI3K/Akt pathway.